IndraLab

Statements


TNF increases the amount of COPS5. 13 / 13
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"NF-κB pathway activated by TNF-α induced CSN5 expression to stabilize PD-L1 expression in cancer cells. xref Palmitoylation of PD-L1 at C272 by DHHC3 blocked mono-ubiquitination of PD-L1 and the subsequent ESCRT-mediated trafficking to multivesicular bodies (MVB), resulting in suppression of PD-L1 lysosomal degradation. xref "

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"In addition, Lim et al. found that TNF-α upregulates the expression of ubiquitin enzyme CSN5, which reduces the ubiquitination of PD-L1 and stabilizes its expression (41)."

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"Mechanistically, TNF-alpha may activate NF-kappaB and induce CSN5 expression, leading to PD-L1 stabilization."

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"It was reported that TNF-α can promote the transcription of CSN5 through activation of the NF-κB signaling pathway."
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"TNF-alpha Upregulates CSN5 Expression to Stabilize PD-L1."

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"Proinflammatory cytokine TNFalpha, secreted by M2 macrophages, induces CSN5 expression through IKKbeta and NF-kappaB activation."

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"Among the 52 deubiquitinating enzymes identified, CSN5, which possesses enzyme activity in the COP9 signalosome, was robustly expressed in response to TNF-alpha treatment in three cell lines examined (XREF_FIG)."

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"TNFalpha upregulates CSN5 expression through activation of the transcription factor NF-kappaB p65, which directly transactivates the promoter of the CSN5 encoding gene."

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"The pro-inflammatory cytokine TNF-α induces the expression of the deubiquitinase CSN5 which deubiquitinates PD-L1 for stabilization (Figure 3), revealing a novel mechanism of immune escape under chronic inflammatory microenvironment [231]."
| PMC

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"TNF-α induces the expression of CSN5 and CSN2 by activating p65 of NF-κB [73]."

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"It was found that TNF stimulation led to the translocation of p65 into the nucleus, where it was stabilized, and activated the transcription of CSN5, which was functionally required for the PD-L1 regulation."

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"The results suggested that TNF-alpha upregulates expression of CSN5, which interacts and deubiquitinates PD-L1 for protein stabilization."

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"Expression of CSN5 mRNA was induced by TNF simulation and was dependent on the NF-κB subunit RelA/p65, which directly regulated CSN5 expression by binding to its promoter."